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1 Department of Sport, ABSTRACT Castellani, John W., Carl M. Maresh, Lawrence E. Armstrong,
Robert W. Kenefick, Deborah Riebe, Marcos Echegaray, Douglas Casa, and
V. Daniel Castracane. Intravenous vs. oral rehydration: effects on
subsequent exercise-heat stress. J. Appl.
Physiol. 82(3): 799-806, 1997.
core temperature; sweat; norepinephrine; cortisol
INTRODUCTION PRESENTLY, FLUID REPLACEMENT after dehydration via
intravenous infusion is based on clinical manifestations of symptoms
and/or the perception that intravenous fluids restore lost body
water more effectively than does oral ingestion. However,
whether the direct administration (intravenous) of fluid to the
intravascular space at rest, after dehydration, helps offset the
deleterious effects of hypohydration better than oral ingestion during
a subsequent exercise bout is not known. For individuals who often
engage in two or more prolonged exercise-heat stress bouts in 1 day
(athletes, soldiers, industrial laborers), it is important to identify
the most efficacious means of rehydration between exercise sessions. If
exercise is initiated in a hypohydrated state or plasma volume (PV) is
not adequately restored, it could lead to higher heart rates (HRs),
higher core temperature (Tco)
values, and decreases in aerobic exercise time (33).
Only one study (18) has compared intravenous infusion with oral
ingestion, with use of fluids replaced during exercise. It was found
that HR was lower in intravenous infusion vs. oral ingestion after
subjects cycled for 2 h. However, direct comparison between those two
treatments was difficult because glucose (18%) was present in the
intravenous trial only and there were large differences (1,000 ml) in
the volume of fluid given between treatments. Other
studies of intravenous saline infusion have compared it with no fluid
ingestion, only during exercise (8, 28). Oral studies have demonstrated
that 2 h of drinking (replacement of 60-65% lost fluids), after
thermal or exercise-induced dehydration, fully restores PV (29),
improves PV by 5-6.5% (7, 22), and normalizes exercising HR to
predehydration values (7). Data are not available that directly address
whether exercise performance, 1-2 h postrehydration, is similar
between intravenous and oral fluid replacement strategies.
Therefore, the purpose of this study was to answer the question, After
exercise-induced dehydration, does rehydration with intravenous
infusion, vs. oral ingestion, differentially affect cardiovascular,
thermoregulatory, and stress hormone variables during subsequent
exercise? Intravenous 0.45% NaCl was chosen as the rehydration fluid
because this is commonly administered to dehydrated individuals. A
similar type and volume of fluid was given orally. Because the period
of rehydration (replacement of 62% of lost fluids) plus rest between
exercise bouts was 2 h, it was hypothesized that PV restoration and
change ( METHODS
This study
compared the influence of intravenous vs. oral rehydration after
exercise-induced dehydration during a subsequent 90-min exercise
bout. It was hypothesized that cardiovascular, thermoregulatory, and hormonal variables would be the same between intravenous and oral rehydration because of similar restoration of
plasma volume (PV) and osmolality (Osmo). Eight non-heat-acclimated men
received three experimental treatments (counterbalanced design) immediately after exercise-induced dehydration (33°C) to 
4%
body weight loss. Treatments were intravenous 0.45% NaCl (iv; 25 ml/kg), no fluid (NF), and oral saline (Oral; 25 ml/kg).
After rehydration and rest (2 h total), subjects walked at 50% maximal
O2 consumption for up to 90 min at
36°C. The following observations were made: 1) heart rate was higher
(P < 0.05) in Oral vs. iv
at minutes 45, 60, and
75 of exercise;
2) rectal temperature, sweat rate, percent change in PV, and change in plasma Osmo were similar between iv
and Oral; 3) change in plasma
norepinephrine decreased less (P < 0.05) in Oral compared with iv at minute
45; 4) changes in plasma adrenocorticotropic hormone and cortisol were similar between iv
and Oral after exercise was initiated; and
5) exercise time was similar between
iv (77.4 ± 5.4 min) and Oral (84.2 ± 2.3 min). These data
suggest that after exercise-induced dehydration, iv and Oral were
equally effective as rehydration treatments. Thermoregulation, change
in adrenocorticotropic hormone, and change in cortisol were not
different between iv and Oral after exercise began; this is likely due
to similar percent change in PV and change in Osmo.
) in osmolality (Osmo) would be similar between treatments
because of adequate gastric emptying and intestinal absorption, leading
to no differences in any of the measured physiological variables during
subsequent exercise.
O2 max), 57.9 ± 1.6 ml · kg
1 · min1;
and percent body fat, 7.7 ± 0.9%. Subjects signed informed consent statements after attending a briefing meeting. All subjects completed a
medical history questionnaire. All procedures were approved by the
Institutional Review Board at the University of Connecticut. Subjects
were paid for their participation.
O2 max.
Briefly, subjects ran at a constant pace (160-220 m/min) for 4 min
at a 0% grade. After 4 min, the grade was increased to 4% for 2 min.
The grade was then increased 2% every 2 min until the subject reached
exhaustion.
4% of their Pre-Dh body weight.
The Dh protocol consisted of alternating cycle ergometry (model 818E,
Monark) and treadmill walking (Quinton, Seattle, WA) in intervals of 25 min of exercise and 5 min of rest. Body weight was measured during each
rest break. Urine was collected throughout Dh and was included as part
of the weight loss. Subjects continued exercising until the desired
weight loss was achieved. The last exercise mode before the 4%
weight loss was always walking to ensure an upright posture. The mean
percent O2 max during
Dh for the three treatments was 50.8 ± 0.2%. The mean temperature and percent relative humidity were 33.0 ± 0.1°C and 47.6 ± 0.5%, respectively. Airflow was 2.3 m/s. HR and rectal
temperature (Tre) were measured
during Dh to ensure the subject's safety.
After Dh, subjects were removed from the chamber and reclined in a
semirecumbent position at 25.5 ± 0.2°C. After 15 min, subjects received one of three rehydration treatments (described in
Experimental treatments) over a
45-min period. Each subject received all three treatments
(separated by a minimum of 14 days), and the order of treatments was
randomized. After rehydration, subjects stood for 55 min in the
laboratory and then reentered the environmental chamber.
After the subject stood in the environmental chamber for 20 min, a
blood sample was obtained. The subject then sat down and consumed 1 g
carbohydrate/kg Pre-Dh body wt of a commercial snack product (Skittles,
M and M Mars, Hackettstown, NJ) and 100 ml of distilled, deionized
water. Carbohydrates were given before the second exercise bout to
offset the possible loss of muscle glycogen during Dh.
Subjects voided their bladders, were weighed (preexercise,
minute 0), and then began walking at
~50% O2 max. Walking speed was verified for each test with a hand-held tachometer (model 8204-20, Cole-Parmer Instrument, Chicago, IL). The duration of
exercise was intended to be 90 min. The mean temperature and percent
relative humidity were 35.9 ± 0.1°C and 46.6 ± 2.1%,
respectively, for the three treatments. The temperature during exercise
was set higher than during the morning Dh period to simulate an
increase in dry-bulb temperature during the course of a day. Airflow
was 2.3 m/s. No fluids were consumed during the exercise period.
Exercise was terminated if 1)
Tre reached 39.5°C,
2) HR exceeded 180 beats/min for 5 consecutive min, 3) subjects showed
signs of heat illness, 4) subjects
asked to stop, or 5) subjects
completed 90 min of exercise.
Experimental treatments.
All treatments were given over a 45 min period. They were
1) no rehydration fluid (NF),
2) intravenous saline (iv; 0.45%
NaCl, 25°C) infusion, and 3)
oral saline (4°C) drinking (Oral). The iv infusion
was administered in the arm opposite to the indwelling venous cannula
via 21-gauge butterfly cannula. The rate of iv infusion was 0.56 ml · kg1 · min1.
Oral consisted of 4 g of a commercial sugar-free flavored beverage (Kool-Aid) dissolved in 889 ml of 0.45% NaCl and 111 ml of distilled, deionized water. The composition of Oral was 78.6 ± 1.0 meq/l Na+, 0.96 ± 0.02 meq/l
K+, and 2.54 ± 0.07 meq/l
Ca2+. The osmolality was 145.6 ± 1.1 mosmol/kg. Oral was chilled (4°C) for palatability. Fluid
intake (iv and drinking) approximated 25 ml/kg Pre-Dh body wt. This
volume has been shown to be at the upper range for orally ingested
fluids after exercise-induced Dh (28). The iv fluid intake was measured
by weighing saline bags pre- and postinfusion on a scale (model GT8000,
O'Haus, Florham Park, NJ). Oral was weighed before each drink, which
was given every 5 min over a 45-min period. The iv treatment was
administered by a nurse experienced in cannula placement and
intravenous infusion.
Measurements.
HR was obtained at 5-min intervals during exercise by a lead 1 configuration by using a HR monitor (Polar Electro).
Tre (°C) was measured every 5 min during exercise by using a thermistor (model 401, Yellow Springs
Instruments, Yellow Springs, OH) inserted 10 cm past the anal
sphincter. Skin temperature
(Tsk) values (°C) were
measured at 10-min intervals during exercise by using thermocouples (model 409, Yellow Springs Instruments) secured on the chest, arm,
thigh, and calf. Mean Tsk was
calculated from these four sites according to Ramanathan (30). Local
chest sweat rate (SRch; mg · min1 · cm2)
was measured, via resistance hygrometry, at minutes
0 and 10 by using a
commercial dew-point sensor (model B1-102, Bi-Tronics, Guilford, CT).
The capsule (12 cm2) was placed
on the chest 5 cm medial to the left nipple. Whole body sweat rate
(l · min1 · m2)
was determined from pre- and postexercise body weights corrected for
respiratory losses and blood draw volume. Oxygen uptake
(O2; ml · kg1 · min1)
was measured by using open-circuit spirometry (model CPX-D, Medical
Graphics, St. Paul, MN) during exercise at minutes 20, 40, 60, and 80.
Blood was taken at Pre-Dh, postdehydration (Post-Dh), preexercise
(minute 0), and at 15 and 45 min of exercise from an indwelling Teflon
cannula (20 gauge) placed in a superficial forearm vein. The arm was
pendant during blood draws. Before each blood sample, subjects were in
a upright posture for 20 min.
Hematocrit (Hct) was determined in triplicate from whole blood by the
microcapillary technique and corrected for trapped plasma (15).
Hemoglobin (Hb) was measured in triplicate by the cyanmethemoglobin method (Kit 525, Sigma Chemical, St. Louis, MO). Percent change in PV
(%PV) was calculated by using the equation of Dill and Costill (10)
from appropriate Hct and Hb values. %PV values were calculated by
using Post-Dh for initial Hb and Hct values. Post-Dh was used as the
initial point to reflect the effect of the various rehydration
treatments after Dh. Plasma Osmo was measured in triplicate by
freezing-point depression (model 5004 m-osmette, Precision Systems,
Natick, MA). Plasma glucose was determined in triplicate via an
enzymatic technique (model 2003 glucose/lactate analyzer, Yellow
Springs Instruments). Plasma norepinephrine (NE) and epinephrine (Epi)
were determined in triplicate via high-performance liquid
chromatography with electrochemical detection (model 460, Waters,
Milford, MA; Ref. 20). Plasma adrenocorticotropic hormone (ACTH) and
cortisol (Cort) were measured in duplicate by solid-phase radioimmunoassay kits (Coat-a-Count, Diagnostic Products, Los Angeles,
CA). Plasma ACTH and Cort samples were frozen at 80°C before
analysis. All samples for a given subject were analyzed in the same
sample run to eliminate interassay variation. Intra-assay coefficient
of variations were 7.0 ± 5.1 (SD), 19.5 ± 15.1, <5, and
<5% for NE, Epi, ACTH, and Cort, respectively. Hormone
concentrations were corrected for %PV from Post-Dh.
Statistical analyses.
Cardiovascular, thermoregulatory, and blood variables were
analyzed by using a two-way (treatment × time) analysis
of variance with repeated measures. Significant
F-ratios were analyzed post hoc with a
Newman-Keuls analysis. The level of significance was P < 0.05. Data are presented as
means ± SE. Although hydration status before Dh and the time to
dehydrate (see RESULTS) were similar
among treatments, and time of day and posture were controlled, variability in several plasma hormone concentrations was observed at
Pre-Dh and Post-Dh (Table 1). Therefore,
data are presented as change scores from Post-Dh to reflect the effect
of the rehydration treatments.
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RESULTS
O2 max was 51.0 ± 2.0, 51.1 ± 1.8, and 50.4 ± 1.9%
(P > 0.05) for iv, NF, and Oral,
respectively. After Dh (Table 1), there were significant (P < 0.05) differences among
treatments in plasma NE, Epi, and ACTH. Also,
Tre (iv vs. Oral) approached
significance (P = 0.05).
Rehydration.
The volume of intravenous or ingested fluid given during the
rehydration period was 1,890 ± 45, 0 ± 0, and 1,856 ± 65 ml
for iv, NF, and Oral, respectively (P > 0.05, iv vs. Oral). Urine volumes were 60 ± 20 ml, 80 ± 20 ml, and 80 ± 20 ml for iv, NF, and Oral, respectively
(P > 0.05).
Time to exhaustion and
O2 during subsequent
exercise.
There was a significantly (P < 0.05)
lower exercise time for NF (58.9 ± 8.4 min) than for iv (77.4 ± 5.4 min) and Oral (84.2 ± 2.3 min), with no differences between iv
and Oral. The percent O2 max was similar
(P > 0.05) among trials, with the
mean percent O2 max
ranging from 53.0 ± 2.6 to 54.4 ± 2.2%. Metabolic heat production was 334.1 ± 17.5, 339.6 ± 19.4, and 336.1 ± 22.7 W/m2
(P > 0.05) for iv, NF, and Oral,
respectively. Tests were terminated for the following reasons: in iv
three subjects reached 39.5°C, one reached HR > 180 beats/min,
one developed signs and symptoms of heat exhaustion/fatigue, and three
completed 90 min; in NF two subjects reached 39.5°C, four exhibited
signs/symptoms of fatigue, and two completed 90 min; in Oral two
subjects reached 39.5°C, two exhibited signs/symptoms of fatigue,
and four completed 90 min.
HR response to exercise.
HR was significantly (P < 0.05)
higher in NF than iv and Oral at minutes 0, 15, and 30 (Fig.
1). Oral had a similar HR response as NF at
minute 45 and was significantly higher
(P < 0.05) than iv at
minutes 45, 60, and
75.
), no fluid (NF; 
), and oral 0.45%
NaCl (Oral; 
). Values are means ± SE. Post-Dh, postdehydration; Rehyd, rehydration period. Nos. before Ex denote minutes. * NF significantly different from iv and Oral,
P < 0.05. 
Oral
significantly different from iv, P < 0.05.
Temperature responses after rehydration and during exercise. Tre decreased by a similar amount in iv and Oral during rehydration and rest and increased at the same rate during exercise (Fig. 2). In contrast, Tre in NF did not decrease to the same extent after rehydration and was significantly elevated (P < 0.05) throughout exercise, compared with iv and Oral. Mean Tsk values were similar among treatments during exercise (Fig. 2).
), NF (),
and Oral (). Values are means ± SE. Post-Dh is considered reference point for change in rectal temperature. * NF
significantly different from iv and Oral,
P < 0.05.
Whole body sweat rate (l · h
1 · m2)
was 0.53 ± 0.03, 0.53 ± 0.05, and 0.52 ± 0.03 for iv, NF,
and Oral, respectively (P > 0.05). Local SRch
(mg · min1 · cm2)
at minute 10 was 1.705 ± 0.078, 1.671 ± 0.071, and 1.755 ± 0.082 for iv, NF, and
Oral, respectively (P > 0.05).
PV and Osmo after rehydration and during exercise.
PV significantly increased (P < 0.05) by 7-8% after rehydration for iv and Oral and remained at
this increased level throughout exercise (Fig.
3). There were no differences in the
%PV between iv and Oral. PV did not change after rehydration or
during exercise in NF and was lower (P < 0.05) than in iv and Oral. Osmo was significantly different
(P < 0.05) in NF compared with iv
and Oral after rehydration and during exercise (Fig. 3) with no
differences between iv and Oral.
), NF (), and Oral (). Values are means ± SE. Post-Dh is
considered reference point. * NF significantly different from iv
and Oral, P < 0.05.
Plasma NE and Epi after rehydration and during exercise.
NE was similar among treatment groups at minute
0 (Fig. 4). NE was
different during NF (P < 0.05) at
minutes 15 and
45 compared with iv and Oral. Also, at
minute 45, NE was significantly
(P < 0.05) different in Oral
compared with iv. No differences in Epi were found among NF, iv, and
Oral (Fig. 4).
), NF (), and
Oral (). Values are means ± SE. Post-Dh is considered reference
point. * NF significantly different from iv and Oral, P < 0.05. Oral
significantly different from iv, P < 0.05.
Plasma ACTH and Cort after rehydration and during exercise.
ACTH and Cort were different after rehydration
(minute 0) in iv compared with Oral;
i.e., change in plasma levels were less in iv after rehydration (Fig.
5). Once exercise was initiated (minutes 15 and
45), ACTH and Cort, from
Post-Dh, were similar between iv and Oral. For NF, the change in plasma
ACTH paralleled that in Oral at minute
0; however, it did not decrease once exercise began.
Unlike Oral, Cort for NF increased after rehydration and remained
elevated at minutes 15 and
45.
), NF (), and Oral
(). Values are means ± SE. Post-Dh is considered reference point. * NF significantly different from iv and Oral,
P < 0.05. Oral
significantly different from iv, P < 0.05.
Plasma glucose after rehydration and during exercise. Plasma glucose concentrations were similar among treatments at Post-Dh (5.51 ± 0.23, 5.27 ± 0.11, 5.17 ± 0.11 mmol/l), minute 0 (5.03 ± 0.13, 5.21 ± 0.13, 5.11 ± 0.24 mmol/l), minute 15 (6.63 ± 0.27, 7.08 ± 0.44, 6.73 ± 0.56 mmol/l), and minute 45 (5.96 ± 0.50, 7.18 ± 0.26, 5.66 ± 0.29 mmol/l) for iv, NF, and Oral, respectively.
DISCUSSION
This study investigated whether intravenous or oral rehydration during
rest, after exercise-induced dehydration, results in similar
cardiovascular, thermoregulatory, and stress hormone responses during a
subsequent exercise bout in a hot environment (36°C). No previous
studies have directly examined this. Several studies (1, 35) have
addressed the effect of oral rehydration, after dehydration, on a
subsequent bout of exercise. They used long dehydration (days) and
variable rehydration (1- to 5-h) periods, with fluid ingestion either
ad libitum or fixed. Those studies, however, did not address the
challenge of rehydrating between exercise bouts on the same day.
Recently, Melin et al. (23) had individuals exercise (35°C) after
thermal dehydration (2.6% body weight loss over 2-3 h) and
1-h rest. Rehydration was given orally by administration of water just
before (913 ml bolus) or during the exercise period. Hamilton et al.
(18) infused an 18% glucose in water solution (1,224 ml) for 100 min
during exercise (70%
O2 max) at 22°C.
They found that infusion prevented the increases in HR that were seen
with water ingestion alone. However, comparisons of infusion vs.
ingestion are confounded by glucose content and volume given. As in the
oral rehydration studies cited above, the design of this intravenous
study does not allow speculation on the effect of resting intravenous
infusion, after dehydration, on a subsequent exercise trial.
The principal finding of this investigation was the higher HR during exercise after oral rehydration compared with rehydrating with a similar type and amount of iv saline. In fact, the HR response was similar between Oral and NF at minute 45. Therefore, the question is, Why does rehydrating orally result in a higher cardiac frequency compared with iv rehydration? Several mechanisms have been suggested to explain differences in HR both in and out of a hot environment. These include reduced muscle glycogen stores (19), lower blood volume (13, 26), and higher Tco and Tsk (31). Reduced muscle glycogen stores in oral rehydration are unlikely because carbohydrate intake before the study was equal and the time to dehydrate was similar between treatments. Hypovolemia is associated with decreased PV and lower stroke volumes, leading to compensatory increases in HR to maintain cardiac output. However, this study found no differences in PV between iv and Oral. Higher Tco and Tsk result in higher HR due to increases in cutaneous blood flow and pooling, leading to decreased central venous pressure and stroke volume (31), but no differences were found for Tre or Tsk between iv and Oral. Thus it is likely that the greater cardiovascular drift in Oral occurred independently of reductions in blood volume (25) or differences in body temperatures.
The plasma NE concentration in Oral, vs. iv, suggests that greater
sympathetic nervous activity (SNA) contributed to the higher HR
response in Oral. It is well known that HR is elevated by an increase
in SNA (5). Plasma NE is a valid measure of SNA because the rate of NE
spillover into the veins is proportional to the rate of sympathetic
nerve firing (11). Hoffman et al. (21) have observed an increase in SNA
after rats drank. However, this effect is transitory; SNA decreases
soon after drinking is stopped. Therefore, the higher SNA during
exercise seen in the present investigation with oral rehydration is
likely not due to the act of drinking itself, because 75 min elapsed
after drinking before the onset of exercise. It has been suggested that
gastrointestinal distension (2) elevates SNA. Data from Berne et al.
(3) do not support this hypothesis, but in their study only 300 ml of
water were given; in the present investigation 1,900 ml were ingested.
Therefore, the possibility exists that some fluid remained in the
intestine after the oral rehydration treatment and triggered a greater
sympathetic nervous response. However, if this hypothesis is correct,
then it would be expected that the NE in Oral would have been
different at minute 15 also when more
fluid was in the gut, compared with minute
45. Berne et al. also demonstrated that higher plasma
glucose evoked greater muscle SNA after glucose ingestion. They suggest
that higher glucose increases splanchnic vasodilation, which, in turn,
activates the sympathetic nervous system. However, glucose was similar
between iv and Oral at minutes 15 and
45, which suggests no role for plasma
glucose in increasing SNA in Oral.
This investigation found no differences in the changes in Tre, Tsk, or sweat rate between iv and Oral. These data suggest, from a thermoregulatory point of view, that it is not important how fluid is replaced between two prolonged exercise-heat stress periods. Recently, Takamata et al. (37) found that oral ingestion transiently increased skin blood flow and SRch via an oropharyngeal reflex. This was associated with a decrease in esophageal temperature (Tes) and a threshold shift to the left in the SRch-Tes relationship in heated, cell-dehydrated humans. The similar rate of fall in Tre after rehydration in iv and Oral suggests that intravenous infusion may also transiently affect the thermoregulatory center. Further studies are warranted to determine whether intravenous infusion influences sweating and the SRch-Tco relationship to a similar degree as did oral ingestion in cell-dehydrated, heated humans (37). Similar SRch and higher Tre values in NF, compared with iv and Oral, suggest a change in sweating threshold (27) likely mediated by the combination of higher plasma Osmo and lower PV (14, 25, 27, 32) in NF.
Plasma ACTH and Cort did not fall in Oral as significantly as iv after
rehydration (minute 0). One
hypothesis for the smaller ACTH and Cort from Post-Dh in Oral at
minute 0 is the stress associated with
ingesting a large volume of cold (4°C), salty (78 meq/l
Na+) fluid. Stress is associated
with activation of the hypothalamic-pituitary-adrenal axis (38).
However, the large fall in plasma ACTH after the beginning of exercise
(from minutes 0-15) may be due
to the withdrawal of the stress induced by fluid
ingestion. ACTH is now likely controlled by other
physiological factors such as %PV, Osmo, or glucose. Because no
differences existed between iv and Oral for these variables, similar
responses were observed in ACTH and Cort after exercise was
initiated. Results from previous exercise studies that compared hormonal responses between NF and fluid replacement treatments (4, 9)
suggest that differences in either PV or plasma Osmo may account for
the higher plasma Cort concentrations during exercise. The pattern seen
in the NF trial (elevated ACTH and Cort) lends further support to the
hypothesis that lower PV or higher Osmo mediates plasma Cort. Glucose
does not appear to have an influence on ACTH and Cort because glucose
concentrations did not fall below 3.3 mmol/l, the threshold needed to
activate hypothalamic-pituitary-adrenal axis hormones during exercise
(36). Further studies are warranted to determine the independent role
of PV and Osmo before and during exercise-heat stress on plasma stress
hormones.
In summary, this study demonstrates that Oral, after exercise-induced
Dh, results in a higher HR during subsequent exercise in the heat
compared with iv. PV was not different between treatments, but it was
observed that the plasma NE concentration was different in Oral
during exercise. This suggests that an augmented sympathetic nervous
system response in Oral was responsible for the higher HR observed in
that trial. Similar responses in thermoregulatory variables between iv
and Oral suggest that both rehydration treatments were equally
effective in restoring lost body fluids for use during subsequent
exercise. ACTH and Cort concentrations in NF suggest that PV and
Osmo mediate plasma concentrations of these hormones.
ACKNOWLEDGEMENTS
The authors thank Mike Whittlesey, Stavros Kavouras, Dane McFarland, Dean Aresco, Nicole Johnson, and Marie Kenefick (Univ. of Connecticut) and Terry Gimpel (Texas Tech) for their technical support. We also thank our subjects for their participation.
FOOTNOTES
Address for reprint requests: J. W. Castellani, Thermal and Mountain Medicine Division, US Army Research Institute of Environmental Medicine, Natick, MA 01760-5007.
Received 6 March 1996; accepted in final form 6 November 1996.
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